The healthy lung defends itself constantly against powerful physical forces tending to cause alveolar collapse, by maintaining a thin film of unusual composition at alveolar air-liquid interfaces through the lung. Present evidence suggests this lining must be constantly renewed, that healthy cells of the alveolar lining are capable of generating the surface active materials (SAM) at an appropriate rate, and that a variety of disease states are associated with extensive alveolar collapse suggesting some abnormality of the "surfactant system." Functionally inadequate lining films might result from either the presence of interfering substances in the alveolar surfaces, or the failure of lung cells to deliver normal supplies of the lining material to alveolar surfaces. Our objective is to study factors which influence the delivery of SAM to alveolar surfaces. We will measure the amount and specific activity of the major lipid component, dipalmitoyl lecitin, recoverable by lavage of the air spaces after pulse-labelling with 14C-1-palmitate, 14C-16-palmitate and 3H-9, 10-palmitate in health and following a variety of physiological, pharamacological, and environmental interventions. We will distinguish between newly-made SAM in lung tissues, and in lung lining fluids, and will relate changes in the availability and distribution of SAM to physiological indices of alveolar stability and to changes in lung morphology at the light and electron microscopic level.